Herpes simplex keratitis is the most prevalent severe ocular infection in this country. The propensity of this infection to recur throughout life and to produce irreversible structural alterations of the cornea and intra-ocular structues results in considerable visual morbidity, medical expense and loss of productivity of otherwise healthy individuals. Currently effective therapy of herpes simplex keratitis is directed only at control of the replicating virus in the cornea. Topical therapeutic agents do not reduce the incidence or severity of stromal keratitis, or other ocular complications. There is no method of blocking access of the virus to the latency site or preventing recurrent shedding of virus and consequent herpetic keratitis. The key to the control of this debilitating disease appears to be knowledge and subsequent control of the mechanism of reactivation. It has recently been determined that passage of current (via an electrode implant) through the trigeminal nerve of rabbits persistently infected with herpes simplex virus elicits rapid release of virus at the eye. This study will refine and develop the electrode model for induction of multiple episodes of virus shedding in the same host, in order to investigate the self-perpetuating aspect of recurrent ocular herpes and to determine whether recurrent disease can be modulated by either drug therapy or host immune factors. Labelled specific antisera to virus coded polypeptides will be used as probes to identify and examine active areas in ganglia from persistently infected and induced animals.